Friday, November 30, 2012

Kidney Function and Bone Mineral Density

Chronic Kidney Disease (CKD) is the progressive loss of renal function. It is most common among older people and those with high blood pressure and/or diabetes.  Early stages can be detected through routine lab tests. As kidneys slowly lose their ability to excrete waste products, urine protein and serum creatinine levels rise - and urine pH drops (Nakanishi et al., 2012). For the 10 to 15% of Americans experiencing CKD, the risk of bone fracture is significantly higher as well. 

Here’s the connection: 
In addition to the important functions of waste excretion and body pH regulation, healthy kidneys produce calcitriol (1,25(OH)2D), the active form of vitamin D that helps the body absorb dietary calcium into the blood and the bones. Even slight kidney impairment can slow this conversion of vitamin D to calcitriol. The less calcitriol in the blood, the less calcium will be absorbed from the food you eat or supplements you take. If calcium absorption drops, levels in the blood become too low. This low blood calcium is detected by sensors in four small parathyroid glands in the neck and triggers their release of a hormone called parathormone (PTH). This hormone draws calcium from the bones to raise blood calcium levels. Too much PTH in the blood (a condition called hyperparathyroidism) will remove excessive amounts of calcium from the bones. Over time, this constant removal of calcium will speed up the loss of bone mineral density (BMD) and increase the risk of bone fracture. Insuring adequate levels of vitamin D intake will help avoid this release of PTH but in individuals with CKD there still may be poor conversion to the active form of D.
There are a number of research studies underway to identify how to reduce or reverse the negative effects on bone for CKD patients.
 
In a study published in the American Journal of Clinical Nutrition researchers (Alvarez et al., 2012) explored whether high doses of vitamin D3 (cholecalciferol) in patients with early CKD (stages 2 and 3) was sufficient to maintain optimal vitamin D status (greater than 30 ng/ml) and to prevent the rise of blood PTH levels. Forty-six subjects were supplemented with 50,000 IU oral vitamin D3 each week for 12 weeks followed by 50,000 IU every other week for 40 weeks. After one year, the authors concluded that this "regime was safe and sufficient to maintain serum 25(OH)D [vitamin D] concentrations and prevent vitamin D insufficiency in early CKD. 

Furthermore, serum PTH improved after cholecalciferol treatment, particularly in patients who had secondary hyperparathyroidism." It appears that by flooding the body with high doses of vitamin D the kidneys are able to produce more active vitamin D. With more of this active form, signaling of the parathyroid glands to release more PTH is turned off.
 
In addition to the compromised ability to activate vitamin D and excrete wastes, as kidney function decreases in CKD patients demonstrate low-grade, chronic metabolic acidosis. Their low urine pH is a reflection of this acidotic state. Alkalinizing potassium* and magnesium supplementation are helpful for increasing body pH levels. Additionally, sources high in the amino acid glutamine (such as whey protein) that is used by the body to produce bicarbonate, the body's most important buffering compound, is helpful in neutralizing acidosis. 
If your kidney function is compromised, be sure to speak with your medical provider about this important aspect of your treatment.
* Note:  Excessive intake of potassium in patients with kidney disease can lead to hyperkalemia, a serious medical condition that can lead to abnormal heart rhythms. If you have kidney disease, consult with your physician before taking supplemental potassium. 
Nakanishi et al. 2012. Low urine pH is a predictor of chronic kidney disease. Kidney and Blood Pressure Research 35(2):77-81.
Alvarez et al. 2012. High-dose cholecalciferol reduces parathyroid hormone in patients with early chronic kidney disease: a pilot, randomized, double-blind, placebo-controlled trial. American Journal of Clinical Nutrition 96(3):672-679.
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